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Depression is a common mental health disorder and is the leading cause of disability worldwide. Gastrodia elata (G. elata) was demonstrated to exhibit a neuroprotective effect in the authors' previous study. The present study investigated the effect of polysaccharides from G. elata (GEP) on PC12 cell apoptosis induced by corticosterone (CORT) and its possible underlying mechanisms. PC12 cells were treated with 200 µM CORT in the absence or presence of different concentrations of GEP for 48 h. Then, cell viability was measured by CCK‑8 assay. The lactate dehydrogenase (LDH) leakage was quantified using an LDH assay kit. The apoptosis degree of the PC12 cells and the morphology was measured by DAPI staining. Subsequently, intracellular ROS level was detected by using DCFH‑DA method, the morphology staining of the endoplasmic reticulum in PC12 cells was determined using the cationic probe, and levels of five proteins involved in apoptosis, i.e., glucose‑regulated protein, 78k Da (GRP78), X‑box binding protein 1 (XBP‑1), growth arrest‑ and DNA damage‑inducible gene 153 (GADD153), caspase 9 and caspase 12 were determined by western blotting. The results demonstrated that treatment with 1,000 µg/ml GEP prior to 200 µM CORT exposure significantly protected the PC12 cells from CORT‑induced cell apoptosis, and reduced levels of LDH leakage and intracellular reactive oxygen species. In addition, pretreatment with GEP inhibited the activation of GRP78, X‑BP‑1, GADD153, caspase 9 and caspase 12. These findings suggested that GEP exhibited a neuroprotective effect against CORT‑induced apoptosis in PC12 cells, and the underlying molecular mechanisms were dependent on inhibition of the endoplasmic reticulum stress‑mediated pathway. This provides novel insight into the effect of GEP when used for the treatment of diseases of the nervous system.

molecular medicine reports

Neuroprotective effect of polysaccharides from Gastrodia elata blume against corticosterone‑induced apoptosis in PC12 cells via inhibition of the endoplasmic reticulum stress‑mediated pathway